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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Minimal Change Disease (MCD) is a major cause of nephrotic syndrome characterized by podocyte injury mediated through immune dysregulation. Myasthenia Gravis (MG) is a rare antibody-mediated autoimmune disease that disrupts neuromuscular transmission, frequently associated with thymic abnormalities. Both conditions represent distinct but overlapping immune pathologies. To describe the clinical course of a patient with refractory MCD complicated by generalized MG, treated successfully with telitacicept. Telitacicepta recombinant fusion protein that combines the extracellular domain of the transmembrane activator and CAML interactor (TACI) with the Fc portion of human IgG. It simultaneously blocks two key B-cell activating factors: BAFF (B-cell activating factor) and APRIL (A proliferation-inducing ligand).
A 68-year-old male with stage III generalized and treated with methylprednisolone and azathioprine 50 mg bid for 4 years. MG symptoms had largely stabilized by the time of admission to our department.3 months ago, the paitients presented nephrotic syndrome and received renal biopsy, renal pathology shown MCD and acute tubular necrosis, was treated with methylprednisolone (40 mg/day). However, the patient remained severely proteinuric with recurrent edema after methylprednisolone for 1 month. Importantly, the lack of response to corticosteroids may be partly attributable to steroid resistance, likely secondary to long-term corticosteroid exposure for MG management. So the paitient recived weekly subcutaneous injections of telitacicept 160 mg once weekly and stop using azathioprine after telitacicept initiation.
After telitacicept initiation, the patient experienced marked reduction in edema. Proteinuria decreased from 15.3 g/day to 0.104 g/day within 2 month, while serum albumin levels increased. Neurological function improved with reduction in quantitative MG (QMG) score, without myasthenic crisis. No severe infections or adverse events were observed.
This case highlights the therapeutic potential of telitacicept in overlapping autoimmune conditions. By targeting BAFF and APRIL pathways, telitacicept may provide dual benefits in controlling renal autoimmunity and antibody-mediated neuromuscular dysfunction.
